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Synthesizes platelet-endothelium mechanisms in thrombosis and repair; extends research framework but leaves clinical translation open.
The recognition that the restoration of patency to occluded blood vessels can improve clinical outcomes has led to intense interest in the formation and dissolution of platelet thrombi and in the pathobiologic features of vascular repair after an injury. To study these events in an experimental model, many investigators challenge isolated platelets or endothelium with stimuli that represent physiologic or pathologic mediators, such as thrombin or adenosine diphosphate (ADP), and find that these agonists cause the generation of intracellular mediators that can markedly alter the function of each cell type. A critical facet of thrombus formation and vascular response to . . .
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Flier et al. (1993) studied this question.
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